Adrenergic influence on pentagastrin and bethanechol stimulated gastric acid secretion in dogs with gastric fistula.

The purpose of this study was to elucidate the effect of alpha-, beta- and dopaminergic receptor stimulation and blockade on pentagastrin and bethanechol stimulated gastric acid secretion in conscious dogs with gastric fistula. Gastric acid secretion was found to be subject to a dose related inhibition by isoprenaline. The dose of isoprenaline producing approximately 50% inhibition was higher in the bethanechol--than the pentagastrin experiments (0.10 vs. 0.03 micrograms/kg/min.) and slightly lower after parietal cell vagotomy. The antisecretory effect was mediated via the beta 1-receptors alone. The inhibitory effect of isoprenaline on pentagastrin stimulated acid secretion showed the characteristics of competitive type and on bethanechol stimulated acid secretion of non competitive type. An increasing and dose-dependent stimulation of bethanechol stimulated gastric acid secretion was found for dopamine 1, 5 and 10 micrograms/kg/min. Dopamine (40 micrograms/kg/min.) exerted an inhibitory effect on pentagastrin and bethanechol stimulated gastric acid secretion mediated, via the beta 1-receptors. The stimulatory effect of low doses of dopamine during bethanechol stimulation could not be defined as an effect via beta-receptors. This dual response, the weak inhibitory effects and the potent decreasing effect on antral gastric motility indicate that dopamine has no physiologic relevant effect on gastric acid secretion. One may conclude that beta 1- and beta 2-receptors may exert an influence on gastric acid secretion in dogs. The main effect of dopamine seems to be on gastric motility, while the effect on gastric acid secretion is of minor importance.